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Folia Microbiol (Praha). 2003;48(4):529-33.

Lack of efflux mechanism in a clinical isolate of Pseudomonas aeruginosa highly resistant to beta-lactams and imipenem.

Author information

1
Microbiology Division, Faculty of Pharmacy, King Saud University, Riyadh, Saudi Arabia. akadry@ksu.edu.sa

Abstract

An isolate of Pseudomonas aeruginosa from cystic fibrosis was highly resistant to beta-lactams and beta-lactamase inhibitors. The resistant determinants of clinical isolate to imipenem, ceftazidim, cefriaxone and cefepime were conjugally nontransferable. The slow or nonenzymically mediated breakdown of imipenem and other broad-spectrum beta-lactams suggested the resistance of P. aeruginosa isolate to these drugs which may be attributed to both permeability and efflux. Impaired penetration of imipenem and other beta-lactams through the membrane was detected by a diminished expression of outer-membrane proteins of approximate molar mass of 46 and 39 kDa, matched to OprD and OprF, respectively. Efflux resistance mechanism for meropenem and beta-lactams has been ruled out since the isolate failed to express outer-membrane protein of approximately 50 kDa which is matched to the OprM protein channel. Thus, reduced permeability in the clinical isolate is the main mechanism conferring resistance against beta-lactams including imipenem.

PMID:
14533486
DOI:
10.1007/bf02931336
[Indexed for MEDLINE]

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